The goal of this research training project is to assess, using cross-sectional and longitudinal analyses, the relationship between near-roadway air pollution (NRAP) and body fat accrual, inflammation, and metabolic dysfunction in a sample of overweight and obese Hispanic or African-American youth. This research training project is designed to expand the applicant, Dr. Stephanie Hsieh's, skills and expertise through mentored research and coursework in the study of neighborhood environmental impacts on human health to include environmental pollutants, and the biological pathways between air pollution and metabolic health. The two specific aims of the proposed research are to: (1) assess cross-sectional associations of residential NRAP exposure and baseline and attained measures in visceral fat, inflammation, and other components of the metabolic syndrome (MetS), controlling for covariates for obesity, and neighborhood contextual variables, and for a sub-set of the CORC sample with repeated measures, (2) investigate longitudinal associations NRAP on one-year change, as well as on one-year attained, visceral fat, inflammation, and other components of MetS. These analyses will be controlled for known covariates of obesity, and baseline neighborhood contextual variables. We will conduct a secondary data analysis of data from a sample of children and youth at the University of Southern California Childhood Obesity Research Center (CORC), who have richly characterized measures of body fat (MRI), inflammation (IL-6 and TNF), and metabolic function (Insulin sensitivity, serum cholesterol, triglycerides). We will layer onto this database data on air pollution, measured as elemental carbon (EC2.5), from the Children's Health Study (CHS) to estimate residential NRAP exposure for each of the CORC participants. Using multi-level (aim 1) and longitudinal (aim 2) statistical models, we will test the following 4 hypotheses: (1) Elevated exposure to EC2.5 at baseline will be associated with increased baseline adipose tissue and increased baseline markers for inflammation and metabolic dysfunction at 1-year follow- up. (2) Elevated exposure to EC2.5 at baseline will result in increased attained obesity and increased markers for inflammation and metabolic dysfunction at 1-year follow- up. (3) Elevated exposure to EC2.5 at baseline will result in a steeper trajectory of accrual in adipose tissue and a steeper trajectory in markers for increased inflammation and metabolic dysfunction from baseline to 1-year follow- up. (4) An increase in exposure to EC2.5 from baseline to 1-year follow-up will result in a steeper trajectory of accrual in adipose tissue and a steeper trajectory in markers for increased inflammation and metabolic dysfunction from baseline to 1-year follow- up. Neighborhood contextual variables will be derived from data previously compiled at the CHS, was well as 2000 and 2010 Census data. This research training experience will be augmented by coursework, as deemed appropriate by the project mentors, in physiology and metabolic health, spatial analysis, and environmental health.